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Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation

Günther, Julia K. and Nikolajevic, Aleksandar and Ebner, Susanne and Troppmair, Jakob and Khalid, Sana (2020) Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation. Biology, 9 (5). p. 99. ISSN 2079-7737

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Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. JNK1/2 are not only regulated by ROS—they in turn can also control ROS production. The prooxidant and cell death function of p66Shc requires phosphorylation by JNK1/2. Here, we provide evidence that establishes p66Shc, an oxidoreductase, as a JNK1/2 effector downstream of Rigosertib-induced ROS production, DNA damage, and cell death. This may provide a common pathway for suppression of tumor cell growth by Rigosertib.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Günther, Julia K.
Nikolajevic, Aleksandar
Ebner, Susanne
Troppmair, Jakob
Khalid, Sanasak242@pitt.edusak242
Date: 15 May 2020
Date Type: Publication
Journal or Publication Title: Biology
Volume: 9
Number: 5
Publisher: MDPI AG
Page Range: p. 99
DOI or Unique Handle: 10.3390/biology9050099
Schools and Programs: School of Dental Medicine > Dental Science
Refereed: Yes
Uncontrolled Keywords: p66Shc, Rigosertib, reactive oxygen species, cell death
ISSN: 2079-7737
Official URL:
Funders: Krebshilfe Tirol
Article Type: Research Article
Date Deposited: 25 May 2021 19:35
Last Modified: 25 May 2021 19:35


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